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Metabolic Myopathies Discovered During Investigations of Statin Myopathy
Open accessAbstract
The statins have emerged as the dominant class of drug for the treatment of hypercholesterolemia. These medications are generally well tolerated. However, myalgias, the most frequent side-effect, occur in up to 7% of patients. Transaminitis and skeletal myotoxicity, with elevated serum creatine kinase (CK) levels (i.e., >10 times the upper limit of normal), occur with reported frequencies of 1% and 0.1%, respectively. Various hypotheses have been proposed to explain the relationship between statin therapy and the spectrum of muscle dysfunction manifested by myalgia, myopathy, and rhabdomyolysis. Statin-mediatd inhibition of mevalonate metabolism impairs the synthesis of isoprenylated products–the most notable of which is ubiquinone. However, isoprenylation is responsible for the post-translational modification of up to 2% of cellular proteins. Therefore, numerous metabolic pathways are potentially modified by statin-mediated hypoprenylation. Subclinical defects in one or more energy-deriving pathways may be unmasked upon exposure to the pleotropic effects of statins. Such pharmacogenomic synergism may underlie the development of “statin myopathy” in a subset of patients. In this regard, we describe four patients with mutations in the myophosphorylase (PYGM; MIM 232600), myoadenylate deaminase (AMPD1; MIM 102770), and carnitine palmitoyltransferase (CPT2; MIM 600650) genes whose diagnoses became apparent during the course of investigations for statin-induced myalgias and hyperCKemia.
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An increased frequency of pathogenic variants in muscle-disease-associated genes has been reported, with a 13- to 20-fold higher incidence in subjects with severe myopathy compared with the general population.
“An increased frequency of pathogenic variants in muscle-disease-associated genes has been reported,96,112–114 with a 13- to 20-fold higher incidence in subjects with severe myopathy compared with the general population.96,112,113”
From Statin-associated muscle symptoms: impact on statin therapy—European Atherosclerosis Society Consensus Panel Statement on Assessment, Aetiology and Management (2015) · cites this paper as [114]
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Self-citationAn assessment by the statin muscle safety task force: 2014 update
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Metadata
- Authors
- Baker, S. K., Vladutiu, G. D., Peltier, W. L., Isackson, P. J., & Tarnopolsky, M. A.
- Affiliations
- McMaster University Medical Centre (CA)
- University at Buffalo, State University of New York (US)
- Medical College of Wisconsin (US)
- Venue
- Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques
- Publisher
- Cambridge University Press (CUP)
- Published
- 2008-03
- Volume
- 35
- Issue
- 1
- Pages
- 94-97
- ISSN
- 0317-1671 (ISSN-L)
- 2057-0155
- OpenAlex
- W2048027661
- Cited by
- 31
- References
- 42
- Citations by year
- 2024: 1 · 2020: 4 · 2019: 3 · 2018: 2 · 2016: 2 · 2015: 4 · 2014: 5 · 2013: 1
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Keywords
- statin-induced myopathy, metabolic myopathies, myophosphorylase deficiency, myoadenylate deaminase deficiency, statin-induced myalgia, rhabdomyolysis, mevalonate metabolism, isoprenylation, pharmacogenomics, hypercholesterolemia
- MeSH terms
- Aged, Alleles, Creatine Kinase, DNA, Humans, Hypercholesterolemia, Male, Metabolic Diseases, Middle Aged, Muscular Diseases, Mutation, Neurologic Examination, Pyridines, Pravastatin, Protein Prenylation, Hydroxymethylglutaryl-CoA Reductase Inhibitors
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